Showing papers by "Richard A. Jorgensen published in 1996"
TL;DR: The degree ofcosuppression observed in progeny of transgenotes carrying multiple, dispersed copies as compared to that observed with a single copy of the transgene suggests that sense cosuppression ofChs is subject to a transgenes dosage effect.
Abstract: Flower pigmentation patterns were scored in 185 senseChalcone synthase (Chs) transgenotes and 85 antisenseChs transgenotes; upon first flowering, 139 (75%) of sense transgenotes were found to be phenotypically altered, as were 70 (82%) of the antisense transgenotes. The observed patterns document the range of phenotypic variations that occur, as well as confirm and extend the finding that senseChs constructs produce several types of morphologybased based flower pigmentation patterns that antisenseChs constructs do not. Long-term monitoring for epigenetic variations in one population of 44 senseChs transgenotes showed that 43 (98%) were capable of producing a cosuppression phenotype. The primary determinant of sense-specific patterns of cosuppression ofChs was found to be the repetitiveness and organization pattern of the transgene, not ‘position effects’ by, or ‘readthrough’ from, flanking plant DNA sequences. The degree of cosuppression observed in progeny of transgenotes carrying multiple, dispersed copies as compared to that observed with a single copy of the transgene suggests that sense cosuppression ofChs is subject to a transgene dosage effect.
433 citations
01 Jan 1996
TL;DR: Sense suppression is observed frequently in transgenic plants, generally as a paradoxical outcome of attempts to increase expression of an endogenous gene by the introduction of a chimeric transgene comprised of a strong promoter fused to a copy of the endogene’s coding sequence in the sense orientation.
Abstract: Plant transgenes can suppress the expression of homologous genes in at least two ways. One is a phenomenon known as epigene conversion,whereby one copy of a gene causes the transcriptional silencing of another copy, and the altered expression state of the silenced gene is heritable after loss of the gene causing the silencing (as in paramutation). The other mode of homology-dependent gene silencing is best referred to as sense suppression, a posttranscriptional phenomenon usually resulting in the cosuppression of homologous transgenes and endogenes. The homology required for sense suppression can be limited to the transcribed regions of the genes. Sense suppression is observed frequently in transgenic plants, generally as a paradoxical outcome of attempts to increase expression of an endogenous gene by the introduction of a chimeric transgene comprised of a strong promoter fused to a copy of the endogene’s coding sequence in the sense orientation. The varied observations and possible mechanisms for homology-dependent transgene silencing phenomena in plants have been much discussed in the literature, citations to which may be found in Matzke and Matzke (1995), de Carvahlo Niebel et al. (1995), and Jorgensen (1995).
7 citations
TL;DR: In flowering plants, transformation with a transgene whose coding sequence is homologous to an endogenous plant gene, and whose expression is driven in the sense orientation by a strong promoter, often produces the opposite outcome of that which was intended, resulting in a null phenotype.
Abstract: In flowering plants, transformation with a transgene whose coding sequence is homologous to an endogenous plant gene, and whose expression is driven in the sense orientation by a strong promoter, often produces the opposite outcome of that which was intended. Instead of over-expression of the gene product, transcripts from both the endogenous gene and the transgene are found to be “cosuppressed,” resulting in a null phenotype. Nuclear run-on experiments have shown that the cosuppressed state is posttranscriptional; experiments that alter transgene dosage suggest that the induction of cosuppression is threshold-dependent; and cytoplasmic RNA viruses that are homologous to a strongly expressed nuclear gene are subject to cosuppression, suggesting that it occurs in the cytoplasm (de Carvalho et al. 1992de Carvalho et al. 1995; Lindbo et al. 1993; Smith et al. 1994; Mueller et al. 1995; Goodwin et al. 1996). A preferred interpretation of these observations, presented in detail by Smith et al. (1994), is that the production of nuclear transcripts to levels exceeding some threshold concentration somehow activates a sequence-specific turnover process that acts in the cytoplasm. This phenomenon is referred to variously as “sense suppression,” “sense cosuppression,” or simply “cosuppression.” It can be distinguished from promoter-homology-dependent suppression, a gene silencing phenomenon that occurs at the transcriptional level, requires promoter homology, and is thought to be a consequence of ectopic pairing (for review, see Matzke and Matzke 1995; see also Vaucheret et al.; Meyer; both this volume). Sense cosuppression also can be distinguished from suppression caused by antisense transgenes (Jorgensen et al. 1996).
4 citations